Retinal venous occlusion is among the foremost causes of sudden painless loss of vision and the second most prevalent retinal vascular disease after diabetic retinopathy. The rubric retinal venous obstructive disease includes two primary manifestations: branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). Although BRVO and CRVO differ in terms of pathophysiology and clinical course, the shared mechanisms for decreased vision include retinal edema, retinal hemorrhage, retinal ischemia, and vitreous hemorrhage. Eighty percent of retinal vein occlusions are BRVO’s[1]. Associations with BRVO include hypertension, cardiovascular disease, increased body mass index by age 20, and glaucoma[2]. The pathophysiology of BRVO typically originates in the retinal vascular anatomy wherein retinal arteries and veins share a common adventitial sheath. As arteriosclerotic changes develop in the arteries, secondary venous compression results in turbulent blood flow leading to endothelial damage and thrombus formation.